Risk factors for repeated percutaneous transluminal angioplasty of hemodialysis vascular access after initial intervention.

BACKGROUND/AIMS: Percutaneous transluminal angioplasty (PTA) is a significant intervention to deal with occlusion and stenosis of vascular access. The study aimed to explore the risk factors of repeated PTA (re-PTA) after the initial intervention in patients undergoing hemodialysis. METHODS: This retrospective study included 180 patients who underwent successful PTA for the first time between March 2016 and December 2020. Information on demographic, clinical, anatomical, and medication variables was collected. Survival curves were plotted using Kaplan-Meier analysis and the risk factors associated with re-PTA were analyzed using univariate and multivariate Cox proportional hazards analyses. RESULTS: The primary clinical patency rates at 6, 12, and 24 months after PTA were found to be 85.2%, 70.7%, and 58.6%, respectively. The univariate Cox proportion hazards analysis revealed the association of non-antiplatelet agents (HR 2.368 95% CI 1.351 to 4.150, p = .003) and arteriovenous graft (AVG) (HR 2.096 95% CI 1.147 to 3.831, p = .016) with re-PTA. However, only non-antiplatelet therapy showed statistical significance (HR 2.368 95% CI 1.351 to 4.150, p = .003) in multivariate Cox proportional hazards analysis. CONCLUSIONS: Among the patients undergoing hemodialysis, the use of antiplatelet agents was associated with a lower risk of re-PTA. Therefore, the use of antiplatelet drugs may reduce the rates of re-PTA and help in maintaining the patency of vascular access.

Erratum: Immunosuppressive agents versus steroids in the treatment of IgA nephropathy-induced proteinuria: A meta-analysis.

[This corrects the article DOI: 10.3892/etm.2015.2860.].

MiR-200a ameliorates peritoneal fibrosis and functional deterioration in a rat model of peritoneal dialysis.

Peritoneal fibrosis is recognised as the main cause of the technical failure of peritoneal dialysis (PD), and currently, there are no specific and effective anti-fibrosis therapies. We have found that miR-200a is down-regulated in a rat model of PD-related peritoneal fibrosis (PF) and could inhibit transforming growth factor beta 1 (TGF-ß1)-induced epithelial-mesenchymal transition (EMT) in peritoneal mesothelial cells by target ZEB1/2. However, its treatment role in vivo is still largely unclear. In this study, we examined the therapeutic potential for miR-200a on PD-related PF in a rat model of PD induced by daily infusion of 4.25% dextrose-containing dialysate. Male Sprague-Dawley rats were divided into four groups: control group, PD group, PD + miR-agomir-NC group, and PD + miR-200a-agomir group (n = 5 in each group). MiR-200a agomir was delivered into the peritoneum by intra-peritoneal injection on days 10 and 20 after PD. We found that treatment with miR-200a agomir significantly reduced the collagen volume fraction (CVF) of the peritoneum and prevented peritoneal dysfunction. The up-regulation of the EMT marker (decreased E-cadherin and increased α-smooth muscle actin) and extracellular matrix (fibronectin and collagen I) was significantly ameliorated by miR-200a in the PD + miR-200a-agomir group. Furthermore, we demonstrated that miR-200a inhibition of PF in vivo was associated with the suppression of ZEB1 and 2, which were proved to be the target of miR-200a in our previous study. In conclusion, results from the present study suggest that treatment with miR-200a may represent a novel and effective therapy for PD-related PF.

MiR-200a negatively regulates TGF-ß1-induced epithelial-mesenchymal transition of peritoneal mesothelial cells by targeting ZEB1/2 expression.

Although epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells was recognized as the key process of peritoneal fibrosis, which is a major cause of peritoneal failure related to peritoneal dialysis (PD), mechanisms underlying these processes remain largely unknown. In this study, we found that miR-200a was significantly downregulated in peritoneal tissues with fibrosis in a rat model of PD. In vitro, transforming growth factor (TGF)-ß1-induced EMT, identified by de novo expression of α-smooth muscle actin and a loss of E-cadherin in human peritoneal mesothelial cells (HPMCs), was associated with downregulation of miR-200a but upregulation of zinc finger E-box-binding homeobox 1/2 (ZEB1/2), suggesting a close link between miR-200a and ZEB1/2 in TGF-ß1-induced EMT. It was further demonstrated that miR-200a was able to bind to the 3'UTR of ZEB1/2, and overexpression of miR-200a blocked TGF-ß1-induced upregulation of ZEB1/2 and, therefore, inhibited EMT and collagen expression. In contrast, overexpression ZEB1/2 blocked miR-200a inhibition of EMT and collagen expression in HMPCs. In conclusion, miR-200a could negatively regulate TGF-ß1-induced EMT by targeting ZEB1/2 in peritoneal mesothelial cells. Blockade of EMT in HPMCS indicates the therapeutic potential of miR-200a as a treatment for peritoneal fibrosis associated with PD.

Immunosuppressive agents versus steroids in the treatment of IgA nephropathy-induced proteinuria: A meta-analysis.

Immunoglobulin A nephropathy (IgAN) is one of the most common types of primary glomerular disease. Immunosuppressive treatment for patients with IgAN remains controversial. The present meta-analysis aimed to assess the efficacy and safety of various immunosuppressive agents compared with steroids in patients with IgAN and moderate to severe proteinuria. PubMed, EMBASE, Cochrane Library, Chinese National Knowledge Infrastructure, Wanfang, Weipu, Chinese Biomedical Literature Database and Qinghuatongfang were searched for relevant randomized controlled trials (RCTs) published between 1990 and September 2013. All eligible studies (biopsy proven IgA nephropathy, use of immunosuppressive agents) measured urinary protein excretion and proteinuria remission. Data were analyzed with the random effects model using Review Manager. A total of 29 RCTs were included, involving 1,466 patients. Compared with steroids, immunosuppressive agents, including azathioprine [corrected] (AZA) [complete response (CR)/partial response (PR); relative risk (RR), 3.43; 95% confidence interval (CI) 1.92-6.12; P<0.0001], mycophenolate mofetil (MMF) (CR/PR; RR, 2.19; 95% CI, 1.25-3.85; P=0.006) and leflunomide (LET) (CR/PR; RR, 2.64; 95% CI, 1.80-3.86; P<0.00001) resulted in increased partial or complete proteinuria remission. Cyclophosphamide (CTX) resulted in a higher reduction of urinary protein excretion than steroids (SMD, 0.91; 95% CI, 0.41-1.41; P=0.0004)). Compared to CTX, LET showed higher effectiveness (CR/PR; RR, 2.01; 95% CI, 1.08-3.75; P=0.03) with a lower incidence of adverse events. The present meta-analysis, which is based on IgAN patients, suggested that AZA, MMF, LET and CTX are effective in reducing proteinuria levels, with acceptable side effects. Therefore, immunosuppressive agents may be considered promising therapeutic agents for the treatment of IgAN and should be investigated further in large sample size, high-quality studies.

The expression profiling and ontology analysis of noncoding RNAs in peritoneal fibrosis induced by peritoneal dialysis fluid.

Increasing amounts of evidence have indicated that noncoding RNAs (ncRNAs) have important regulatory potential in various biological processes. However, the contributions of ncRNAs, especially long noncoding RNAs (lncRNAs), to peritoneal fibrosis remain largely unknown. The aim of this study was to investigate miRNA, lncRNA and mRNA expression profiles and their potential roles in the process of peritoneal fibrosis. Microarray expression profiles of the miRNAs, lncRNAs and mRNAs were determined in normal control peritoneum and in a mouse model of peritoneal dialysis fluid (PDF)-induced fibrotic peritoneum. Differential expression, pathway and gene network analyses were developed to identify possible functional RNA molecules in peritoneal fibrosis. Compared to the normal control, 232 lncRNAs (127 up-regulated and 105 down-regulated), 154 mRNAs (87 up-regulated and 67 down-regulated) and 15 miRNAs (14 miRNAs up-regulated and 1 down-regulated) were differentially expressed in the fibrotic peritoneum. Among the differentially expressed ncRNAs, 9 lncRNAs and 5 miRNAs were validated by real-time RT-PCR. Pathway analysis showed that the Jak-STAT, TGF-beta and MAPK signaling pathways had a close relationship with peritoneal fibrosis. Gene co-expression network analysis identified many genes, including JunB, HSP72, and Nedd9. It also identified lncRNAs AK089579, AK080622, and ENSMUST00000053838 and miRNAs miR-182 and miR-488. All of these species potentially play a key role in peritoneal fibrosis. Our results provide a foundation and an expansive view of the roles and mechanisms of ncRNAs in PDF-induced peritoneal fibrosis.